The word infarct derives from the latin infarcire, meaning “to stuff”, and was applied to myocardial damage when histologists noted the hypercellularity of the affected area of myocardium. I doubt whether the physicians of the day would venture to tell the patient their heart was “stuffed”, which is presumably a later use of the word, but not necessarily inapplicable. However, we have come a long way from that description and the advent of ever more sensitive biomarkers means that many events we now classify as myocardial infarction (MI) would probably not show this histological change.
In many cases, we have no difficulty deciding whether an MI has taken place but, as a one-time outcomes assessor for a large multicenter trial, I am only too aware that there are many clinical presentations where the diagnosis is contentious. The importance can be critical — for the social and personal circumstances of the patient, the consequent decisions for clinical management, and the results of clinical trials. I attended three sessions at the ESC that focused on the outcome of deliberations of the international task force that developed the third version of the Universal Definition of MI, now published in no fewer than five journals simultaneously. There was plenty to debate.
Two examples that divided the committee were that of a 14-year old with a prolonged episode of supraventricular tachycardia with chest discomfort and a small but qualifying biomarker rise, and an endurance athlete with similar findings.
The emergence of the concept of a “Type-2 MI” in the last iteration of the universal definition (2007) has been useful in restraining cardiologists (and those who would refer to them) from initiating the now default practice of rushing in with treatment appropriate for a “Type-1 MI” (due to plaque rupture) when this is unlikely to have been the pathology. However, during the discussions a number of verbal knots and conceptual gymnastics ensued when trying to differentiate Type-2 MI and myocardial injury. We in the audience were left a little unsure as to whether the latter included the former or if it was a separate category qualified by the term “not due to ischemia.” It was also a moot point whether, in the two patient examples, ischemia could be confidently ruled in or out. When all was said and done, we were exhorted to resort to that crucial but arbitrary deal-breaker of careful clinical judgement.
Another point of contention and change to the previous definition was how much leeway interventionalists may have in not classifying post-procedural rises in troponin as MIs, especially as newer, highly sensitive troponin tests have lowered the values detectable. The new threshold is 5 times the upper limit of normal and supporting evidence was provided that such rises were not of prognostic importance. Surgeons get 10 times the upper limit of normal and at least one audience member wondered if these multipliers weren’t a bit arbitrary.
Among other issues debated was the importance of using a “delta”, or change in levels, as the crucial leverage point for an MI classification, but task-force member Alan Jaffe helpfully (?) pointed out that each troponin assay is different and timing of samples must be standardized for valid comparison. The task force has yet to reach consensus on what the delta needs to be — absolute or percentage change, universal statistic, or different ones at different absolute levels of troponin.
So there’s plenty of “stuff” to keep researchers busy, cardiologists scratching their heads, and the task force in business until version four of the Universal Definition of MI comes around.